Both immune and non-immune mechanisms are involved in muscle damage and dysfunction occurring in idiopathic inflammatory myopathies (IIMs). Crosstalk among inflammatory cells, muscle and endothelial cells is essential in the pathogenesis of IIMs. Resistin, originally described as an adipokine linking obesity and insulin resistance in rodents, has been shown a pro-inflammatory molecule in humans. Besides its direct effect on production of several inflammatory mediators, resistin influences chemotaxis, migration, proliferation, cell survival, endothelial dysfunction and metabolism--all aspects implicated in the pathogenesis of IIMs. Up-regulation of resistin in muscle tissue and elevated serum resistin levels have been recently demonstrated in patients with IIMs. In addition, serum levels of resistin reflected global disease activity, including extramuscular organ involvement, in patients with this disease. However, there are currently not sufficient data to distinguish the features of resistin that cause injury of muscle tissue from those that promote muscle regeneration and repair. The aim of this review is therefore to summarize current knowledge about potential implication of resistin in idiopathic inflammatory myopathies.